| Autor: |
Baez-Jurado E; Departamento de Nutrición y Bioquímica, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá, DC, Colombia., Vega GG; Departamento de Nutrición y Bioquímica, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá, DC, Colombia., Aliev G; Institute of Physiologically Active Compounds Russian Academy of Sciences, Chernogolovka, 142432, Russia.; GALLY International Biomedical Research Consulting LLC, San Antonio, TX, 78229, USA.; School of Health Science and Healthcare Administration, University of Atlanta, Johns Creek, GA, 30097, USA., Tarasov VV; Institute of Pharmacy and Translational Medicine, Sechenov First Moscow State Medical University, 2-4 Bolshaya Pirogovskaya st., 119991, Moscow, Russia., Esquinas P; Facultad Medicina Veterinaria y Zootecnia, Universidad Nacional de Colombia, Bogotá, Colombia., Echeverria V; Facultad Ciencias de la Salud, Universidad San Sebastián, Lientur 1457, 4030000, Concepción, Chile., Barreto GE; Departamento de Nutrición y Bioquímica, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá, DC, Colombia. gsampaio@javeriana.edu.co.; Instituto de Ciencias Biomédicas, Universidad Autónoma de Chile, Santiago, Chile. gsampaio@javeriana.edu.co. |
| Abstrakt: |
Previous studies have indicated that paracrine factors (conditioned medium) increase wound closure and reduce reactive oxygen species in a traumatic brain injury in vitro model. Although the beneficial effects of conditioned medium from human adipose tissue-derived mesenchymal stem cells (hMSCA-CM) have been previously suggested for various neurological diseases, their actions on astrocytic cells are not well understood. In this study, we have explored the effect of hMSCA-CM on human astrocyte model (T98G cells) subjected to scratch assay. Our results indicated that hMSCA-CM improved cell viability, reduced nuclear fragmentation, attenuated the production of reactive oxygen species, and preserved mitochondrial membrane potential and ultrastructural parameters. In addition, hMSCA-CM upregulated neuroglobin in T98G cells and the genetic silencing of this protein prevented the protective action of hMSCA-CM on damaged cells, suggesting that neuroglobin is mediating, at least in part, the protective effect of hMSCA-CM. Overall, this evidence suggests that the use of hMSCA-CM is a promising therapeutic strategy for the protection of astrocytic cells in central nervous system (CNS) pathologies. |
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